Peroxisomal β-oxidation regulates histone acetylation and DNA methylation in <i>Arabidopsis</i>.

Abstract

Epigenetic markers, such as histone acetylation and DNA methylation, determine chromatin organization. In eukaryotic cells, metabolites from organelles or the cytosol affect epigenetic modifications. However, the relationships between metabolites and epigenetic modifications are not well understood in plants. We found that peroxisomal acyl-CoA oxidase 4 (ACX4), an enzyme in the fatty acid β-oxidation pathway, is required for suppressing the silencing of some endogenous loci, as well as <i>Pro35S</i>:<i>NPTII</i> in the <i>ProRD29A:LUC</i>/C24 transgenic line. The <i>acx4</i> mutation reduces nuclear histone acetylation and increases DNA methylation at the <i>NOS</i> terminator of <i>Pro35S</i>:<i>NPTII</i> and at some endogenous genomic loci, which are also targeted by the demethylation enzyme REPRESSOR OF SILENCING 1 (ROS1). Furthermore, mutations in multifunctional protein 2 (MFP2) and 3-ketoacyl-CoA thiolase-2 (KAT2/PED1/PKT3), two enzymes in the last two steps of the β-oxidation pathway, lead to similar patterns of DNA hypermethylation as in <i>acx4</i> Thus, metabolites from fatty acid β-oxidation in peroxisomes are closely linked to nuclear epigenetic modifications, which may affect diverse cellular processes in plants.